Hyponatraemia explained clearly, why sodium is about water, not salt

Hyponatraemia is one of the most common electrolyte abnormalities encountered in hospital practice.

It appears on blood results across medical, surgical, oncology, and critical care settings. It can be mild and incidental. Or it can be life-threatening.

Yet despite how frequently it occurs, hyponatraemia is often misunderstood.

Many clinicians instinctively associate low sodium with “not enough salt.”
In reality, hyponatraemia is usually a disorder of water balance, not sodium deficiency.

Understanding this distinction changes management entirely.

What Is Hyponatraemia?

Hyponatraemia is defined as:

Serum sodium <135 mmol/L

Severity is often categorised as:

  • Mild: 130–134 mmol/L
  • Moderate: 125–129 mmol/L
  • Severe: <125 mmol/L

But severity of symptoms does not always correlate neatly with the number.

The rate of change matters more than the absolute value.

Sodium reflects water balance

Serum sodium concentration represents the ratio of:

  • Total body sodium
    to
  • Total body water

It does not directly measure total sodium stores.

A useful way to think about it:

If you add water to the body without adding sodium, the sodium becomes diluted.

If you lose sodium and water proportionally, sodium concentration may stay normal.

Therefore, most hyponatraemia occurs because of:

  • Excess water retention
  • Impaired water excretion
  • Inappropriate antidiuretic hormone (ADH) activity

Not because the body has run out of salt.

Why the brain is at risk

Sodium is the primary determinant of extracellular osmolality.

When sodium levels fall:

  • Plasma osmolality decreases.
  • Water shifts into cells.
  • Cells swell.

In most tissues, mild swelling is tolerated.

In the brain, swelling is dangerous.

Because the skull is a fixed space, cerebral oedema can lead to:

  • Headache
  • Confusion
  • Seizures
  • Reduced consciousness
  • Respiratory arrest

Acute hyponatraemia is therefore a neurological emergency.

Acute vs chronic hyponatraemia

The timeline is crucial.

Acute (<48 hours)

  • Brain has not adapted.
  • Higher risk of cerebral oedema.
  • Symptoms more dramatic.
  • May require urgent hypertonic saline.

Chronic (>48 hours)

  • Brain adapts by reducing intracellular osmoles.
  • Symptoms may be mild or absent.
  • Correction must be slow to prevent harm.

Rapid correction of chronic hyponatraemia can cause:

Osmotic demyelination syndrome (ODS)

A devastating neurological complication.

This is why management requires precision.

Step 1: Confirm It’s true hyponatraemia

Before treating, confirm:

  • Serum osmolality
  • Glucose level
  • Triglycerides (if indicated)

Some patients have:

Pseudohyponatraemia

  • Normal osmolality
  • Lab artefact (e.g., severe hyperlipidaemia)

Hypertonic Hyponatraemia

  • High glucose causes osmotic water shift
  • Sodium appears low due to dilution

Treat the underlying issue — not the sodium number alone.

Step 2: Assess Volume Status

Clinically classify the patient as:

  1. Hypovolaemic
  2. Euvolaemic
  3. Hypervolaemic

This guides treatment.

Hypovolaemic Hyponatraemia

Causes:

  • Vomiting
  • Diarrhoea
  • Diuretics
  • Adrenal insufficiency

Mechanism:

  • Loss of sodium and water
  • ADH released in response to hypovolaemia
  • Water retained disproportionately

Treatment:

  • Restore volume with isotonic fluids
  • Address underlying cause

As volume improves, ADH decreases, and sodium corrects.

Euvolaemic Hyponatraemia

Most commonly due to:

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Causes of SIADH:

  • Pulmonary disease
  • CNS pathology
  • Malignancy
  • Certain medications (e.g., SSRIs, carbamazepine)

Mechanism:

  • Inappropriate ADH secretion
  • Water retained
  • Sodium diluted

Treatment:

  • Fluid restriction
  • Treat underlying cause
  • Consider pharmacological therapy if persistent

Giving normal saline in SIADH often worsens hyponatraemia.

Understanding physiology prevents this common mistake.

Hypervolaemic Hyponatraemia

Seen in:

  • Heart failure
  • Liver cirrhosis
  • Nephrotic syndrome

Mechanism:

  • Effective circulating volume is low
  • RAAS and ADH activated
  • Water retained disproportionately

Patient appears fluid overloaded — yet physiologically “underfilled.”

Treatment:

  • Fluid restriction
  • Diuretics
  • Address underlying organ failure

Again, giving more fluid often worsens the problem.

When to Use Hypertonic Saline

Hypertonic (3%) saline is indicated when:

  • Severe symptoms (seizures, coma)
  • Acute hyponatraemia with neurological compromise

Goal:

  • Raise sodium by 4–6 mmol/L initially
  • Relieve cerebral oedema
  • Avoid overcorrection

Maximum correction generally:

  • ≤8–10 mmol/L in 24 hours
  • ≤18 mmol/L in 48 hours

Overcorrection is as dangerous as under-treatment.

Why overcorrection is dangerous

In chronic hyponatraemia, brain cells adapt by reducing osmoles.

If sodium rises too quickly:

  • Water shifts out of brain cells rapidly.
  • Cells shrink.
  • Demyelination may occur.

Osmotic demyelination syndrome can cause:

  • Quadriplegia
  • Dysarthria
  • Locked-in syndrome
  • Death

Correction must be controlled and monitored.

Frequent sodium checks are essential during active management.

Common clinical pitfalls

  • Treating the sodium number without assessing volume status.
  • Giving isotonic saline to SIADH.
  • Overlooking medications as a cause.
  • Correcting too rapidly.
  • Failing to monitor closely.
  • Ignoring mild chronic hyponatraemia (which increases fall risk in elderly patients).

Hyponatraemia is common — but not benign.

Even mild chronic cases are associated with:

  • Cognitive impairment
  • Gait instability
  • Increased fracture risk

A Practical Framework

When faced with hyponatraemia:

  1. Confirm serum osmolality.
  2. Check glucose.
  3. Assess volume status.
  4. Review medications.
  5. Measure urine sodium and osmolality.
  6. Determine chronicity.
  7. Treat underlying cause.
  8. Correct carefully.

This structured approach prevents reactive management.

Why hyponatraemia is a clinical intelligence test

Hyponatraemia requires integration of:

  • Physiology
  • Pharmacology
  • Clinical examination
  • Lab interpretation
  • Risk assessment

It rewards reasoning over reflex.

It punishes assumption.

Understanding that sodium is fundamentally about water balance — not salt deficiency — transforms your approach.

Key Takeaways

  • Hyponatraemia is usually a disorder of water excess.
  • Rate of change matters more than the number alone.
  • Volume status determines treatment.
  • Rapid correction can cause irreversible harm.
  • Always treat the underlying cause, not just the lab value.

Clinical intelligence develops when we move beyond memorising thresholds and begin understanding mechanisms.

Hyponatraemia is an excellent place to practise that skill.

Because in medicine, clarity about physiology is what turns routine lab results into safe, precise care.

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